Deep hypothermic circulatory arrest facilitates repair of complex congenital cardiac anomalies in infants. Susceptibility to ischemia of central nervous tissue, however, remains the major limitation to the technique. Investigations in this laboratory have determined that an obstructive lesion of the cerebral microcirculation ("no-reflow phenomenon") which increases in severity with increasing time of normothermic circulatory arrest is abated for up to one hour by deep hypothermia. However, the precise etiology of the no-reflow phenomenon and its causal relationship to cerebral death has not yet been established. Evidence exists that occlusion of capillaries by aggregates (fibrin, rbc, platelet) cannot account for the microcirculatory lesion. This study is designed to systemtically determine whether the persistent microcirculatory collapse is related to high intracapillary surface tension relative to local reperfusion pressure (critical opening pressure), or to high extravascular pressure (i.e. cellular or interstitial edema). The effect of circulatory arrest and hypothermia on the activities of the enzymes of neuronal sodium and potassium transport, oxidative phosphorylation and lysomes and their relationship to the microcirculatory obstructive lesion will be determined. Mongrel dogs will be subjected to circulatory arrest at normothermia, and following combined surface and core cooling with cardiopulmonary bypass. The distinction between cerebral edema and a high critical opening pressure will be determined by the effect of high reflow perfusion pressures, surface active agents, and high intravascular osmotic gradients, on the development of the no-reflow lesion. The contribution of neuronal dysfunction to the vascular obstructive lesion and vice versa will be determined by comparing enzymic activities and protein synthesis in reperfused versus damaged cerebral tissue.